Ronald C. Ma, MB BChir; Chun Chung Chow, MBBS
Potential Financial Conflicts of Interest: None disclosed.
Ma RC, Chow CC. Thyrotoxicosis as a Risk Factor for Pulmonary Arterial Hypertension. Ann Intern Med. 2006;144:222. doi: 10.7326/0003-4819-144-3-200602070-00022
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Published: Ann Intern Med. 2006;144(3):222.
TO THE EDITOR:
Although Rubin and associates (1) pointed out the importance of assessing patients with pulmonary arterial hypertension (PAH) for underlying autoimmune–collagen vascular disease, the need to assess for thyroid dysfunction and autoimmune thyroid disease was not addressed. Previous studies have suggested a link between primary pulmonary hypertension and autoimmune thyroid disease (2). More recently, it has become apparent that thyrotoxicosis is itself an important risk factor for PAH (3, 4). This may be partly due to the hemodynamic effects of hyperthyroidism because biochemical improvement in thyroid function following treatment has been associated with Doppler echocardiographic evidence of improvement in PAH (3, 5). However, there is also evidence suggesting that thyroid autoantibodies present in autoimmune thyroid disease may have a direct role in the pathogenesis of PAH by contributing to pulmonary vascular endothelial injury. This is supported by a report of pulmonary hypertension associated with neonatal thyrotoxicosis caused by transplacental passage of thyroid-stimulating immunoglobulins; pulmonary hypertension resolved completely after the thyrotoxicosis was treated (6). All patients with PAH should be evaluated for thyroid dysfunction because this may be a readily treatable and reversible cause of the condition.
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